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NOS3 — NOX3

Text-mined interactions from Literome

Yang et al., J Cardiovasc Pharmacol 2000 : We conclude that estrogen increases NOx release in HCAECs, which is independent of cytosolic Ca2+ mobilization and is mediated by the upregulation of eNOS
Kobayashi et al., J Physiol Pharmacol 2001 (Stomach Ulcer) : In addition the expression of cyclooxygenase-2 and inducible nitric oxide synthase proteins increased PGE2 generation and NOx secretion in the ulcerated stomach were suppressed by FR167653
Endres et al., Stroke 2004 (Substance Withdrawal Syndrome) : Rho negatively regulates endothelial nitric oxide synthase and Rac contributes to NAD ( P ) H-oxidase activation and superoxide production
Rask-Madsen et al., Arterioscler Thromb Vasc Biol 2005 (Arteriosclerosis...) : Furthermore, the review summarizes studies that implicate PKC in promoting proatherogenic mechanisms or inhibiting antiatherogenic mechanisms, including studies of endothelial dysfunction ; gene induction and activation of vascular NAD ( P ) H oxidase ; endothelial nitric oxide synthase expression and function ; endothelin-1 expression ; growth, migration, and apoptosis of vascular smooth muscle cells ; induction of adhesion molecules ; and oxidized low-density lipoprotein uptake by monocyte derived macrophages
Polytarchou et al., Eur J Pharmacol 2005 : Superoxide dismutase ( SOD ), tempol ( membrane permeable SOD mimetic ) and the NADPH oxidase inhibitors, 4- ( 2-aminoethyl ) -benzenesulfonyl fluoride and apocynin, but not allopurinol, inhibited HUVEC proliferation and migration, as well as activity of endothelial NOS (eNOS)
Basu et al., Crit Rev Microbiol 2005 : Perturbation of macrophage surface with different bacterial pathogens leads to activate general signal transduction pathways of macrophages, including activation of NADPH oxidase , nitric oxide synthase , and so on
Hu et al., Am J Hypertens 2006 (Hypertension) : In male SD rats, apocynin but not l-arginine prevented and reversed Dex-hypertension, suggesting that NAD ( P ) H oxidase mediated superoxide production but not endothelial nitric oxide synthase uncoupling is important in Dex-hypertension
Oak et al., Diabetes 2007 (Diabetes Mellitus, Experimental...) : Attenuation of angiotensin II signaling recouples eNOS and inhibits nonendothelial NOX activity in diabetic mice
Zhang et al., Arterioscler Thromb Vasc Biol 2008 : Paradoxical activation of endothelial nitric oxide synthase by NADPH oxidase
Besler et al., Expert Rev Cardiovasc Ther 2008 (Atherosclerosis...) : The underlying mechanisms remain largely to be defined ; however, they likely include activation of the PI3-kinase/Akt pathway and endothelial nitric oxide synthase , as well as inhibition of NAD ( P ) H oxidase activity of progenitor cells
Signorello et al., Biochim Biophys Acta 2009 : Thus NO, cGMP and superoxide anion level, the phosphorylation status of nitric oxide synthase , the protein kinase C ( PKC ), and NADPH oxidase activation were measured
McCarty et al., Med Hypotheses 2010 (Atrial Fibrillation...) : Nox2- and Nox4 dependent NADPH oxidase activity appears to be a major source of this oxidative stress, and oxidants can induce conformational changes in xanthine dehydrogenase, nitric oxide synthase , and the mitochondrial respiratory chain which increase their capacity to generate superoxide as well
Ikeda et al., Free Radic Biol Med 2010 : This increase was significantly inhibited by N ( ? ) -nitro-l-arginine ( nitric oxide synthase inhibitor ) and diphenyleneiodonium chloride ( NADPH oxidase inhibitor )
Zanette et al., Toxicol In Vitro 2011 (Necrosis) : Apocynin, NADPH-oxidase inhibitor, or N ( G ) -monomethyl-L-argynine, nitric oxide synthase inhibitor , did not prevent NPs induced reduction of cell viability
Jarajapu et al., Invest Ophthalmol Vis Sci 2011 (Diabetic Retinopathy...) : The authors tested the hypothesis that either increasing eNOS expression or inhibiting NADPH oxidase would restore the reparative function in diabetic EPCs
Schuhmacher et al., Diabetes 2011 (Diabetes Mellitus, Experimental...) : Diabetes is associated with vascular oxidative stress, activation of NADPH oxidase , and uncoupling of nitric oxide ( NO ) synthase ( endothelial NO synthase [eNOS ] )
Shuttleworth et al., J Auton Nerv Syst 1995 : NOx release was inhibited by an inhibitor of nitric oxide synthase activity ( N ( G ) -monomethyl-L-arginine ) or by reduction in extracellular Ca2+ concentration